Changes In NT-proBNP Research Articles

506: Comparison of Impedance Cardiography to Thermodilution Cardiac Output Determination in Pediatric Heart Transplant Patients

LVEF (-2.5%; 95% CI: -3.4, -1.6, P 0.001), lower LVSF-Z (-0.61 SD; 95% CI: -0.88, -0.33; P 0.001), higher LVDD-Z (0.31 SD; 95% CI: 0.15, 0.47; P 0.001), and higher LVSD-Z (0.39 SD; 95% CI: 0.18, 0.60; P 0.001) in that person. Conclusions: NT-proBNP is strongly associated with symptoms and indices of systolic function and cardiac remodelling. Changes in NT-proBNP in children with HF provide a good proxy for the evolution of HF and the response to treatment.

Changes of NT proBNP correlated with the regression of left ventricular hypertrophy in patients with aortic valve replacement

Changes of NT proBNP correlated with the regression of left ventricular hypertrophy in patients with aortic valve replacement

Abstract 1603: Factors and Mechanisms Associated with Improved Cardiopulmonary Performance after Cardiac Resynchronization Therapy. An Exercise Echocardiography Study.

Background: Cardiac resynchronization therapy (CRT) leads to better cardiopulmonary performance in congestive heart failure (CHF) patients (pts). Mechanisms underlying the benefits are not fully elucidated. Aim: To investigate factors and mechanisms associated with improved cardiopulmonary performance after CRT. Methods: Twenty-three pts (EF 26±7%, QRS complex 170±26 msec) were studied by simultaneous quantitative semi-supine exercise echocardiography and cardiopulmonary exercise testing before and 3 months after CRT. Pts with an increase (Δ) in peak VO 2 ≥1.1 ml/kg/min were considered clinical responderes. Effective regurgitant orifice (ERO) of the mitral regurgitation (MR) was assessed using the PISA method. Results: In the entire population, CRT was associated with a decrease in LV dyssynchrony from 53±2 to 23±9 msec (p<0.001), increase LV ejection fraction (EF) from 26±7 to 36±9% (p<0.001) and ERO reduction from 0.24±0.11 to 0.13±0.06 cm 2 (p<0.001) In addition, peak VO 2 increased from 11.6±2.3 to 12.9±3.6 ml/kg/min (p<0.01) and Nt-pro BNP decreased from 2795±1644 to 2021±1353 pg/ml (p<0.05). At follow-up (Table ), ERO at rest was similar but exercise-induced ERO and Nt-pro BNP were significantly lower in responders vs nonresponders. Change in peak VO 2 correlated inversely with the extent of exercise-induced MR at follow-up (r=−0.47, p<0.05), with baseline Nt-pro BNP levels (r=−0.53, p<0.05) and change in LVESV (r=−0.49, p<0.05). Conclusions. Improved cardiopulmonary performance after CRT is related to changes in exercise-induced MR rather than resting MR. Thus, effects on the exercise-induced MR in parallel to reverse LV remodelling appear to contribute to improved cardiopulmonary performance and clinical benefits of the CRT.

Role of NT-proBNP and 6MWD in chronic thromboembolic pulmonary hypertension

This study aims to evaluate the role of NT-proBNP and six minute walking distance (6MWD) in the pre- and post-operative assessment of subjects undergoing pulmonary endarterectomy (PEA) for chronic thromboembolic pulmonary hypertension (CTEPH). Subjects undergoing PEA between August 2004 and July 2006 were assessed at baseline and 3 months post-operatively with resting haemodynamics, NT-proBNP and 6MWD. A number of 111 subjects underwent surgery, of which 102 were included. 15 subjects died before their 3 month assessment. Non-survivors had significantly worse preoperative NT-proBNP and 6MWD (4728 pg/mL vs 1863 pg/mL, p=0.001, 182.4 m vs 263.5 m, p=0.001). Taking pre-operative cut-off values of 1200 pg/mL for NT-proBNP and 345 m for 6MWD, both tests had high negative predictive value for predicting mortality (97.3% and 100%, respectively). Amongst survivors, peri-operative changes in NT-proBNP and 6MWD correlated with changes in total pulmonary resistance (TPR) (r=0.49, p<0.001 and r=-0.46, p<0.001). Post-operatively, both NT-proBNP and 6MWD also correlated with mPAP (r=0.65, p<0.001 and r=-0.50, p<0.001) and PVR (r=0.63, p<0.001 and r=-0.47, p<0.001). The ability of NT-proBNP to predict persistent pulmonary hypertension was significantly confounded by age, but not gender, BMI or renal function. Pre-operative evaluation with NT-proBNP and 6MWD helps risk-stratify patients prior to PEA. Post-operatively, both markers correlate with changes in disease burden and right ventricular function. These results suggest that both NT-proBNP and 6MWD offer effective 'bedside' tools for the long term follow up of patients with CTEPH.

Prognostic importance of plasma NT‐pro BNP in chronic heart failure in patients treated with a β‐blocker: Results from the Carvedilol Or Metoprolol European Trial (COMET) trial

Plasma levels of N-terminal pro-brain natriuretic peptide (NT-pro BNP) are increased in patients with chronic heart failure (CHF). Beta-blockers (BB) may influence these levels but it is unclear whether changes in NT-pro BNP reflect concomitant changes in prognosis. To assess the prognostic importance of NT-pro BNP at baseline and during follow-up, in patients in whom beta-blocker therapy is initiated. In COMET, 3029 patients with CHF in NYHA class II-IV and EF<35% were randomised to carvedilol or metoprolol tartrate and were followed for an average of 58 months. Blood samples were collected for the measurement of NT-pro BNP at baseline (n=1559) and during follow-up (n=309). Baseline plasma concentrations of NT-pro BNP above the median (1242 pg/ml) were associated with higher all-cause mortality (RR 2.77; 95% CI 2.33-3.3, p<0.001). Patients who achieved NT-pro BNP levels<400 pg/ml during follow-up had a lower subsequent mortality (RR 0.32; 95% CI 0.15-0.69, p=0.004). The plasma concentration of NT-pro BNP is a powerful predictor of mortality in patients with CHF. Patients who achieve an NT-pro BNP of <400 pg/ml subsequent to treatment with a beta-blocker have a favourable prognosis.

Rationale and Design for the UNC Duke Acute Decompensated Heart Failure with Hypertension Study (UNDU ADHF-HTN)

Introduction: Registry data indicate that ADHF patients (pts) are commonly hypertensive at admission. In ADHERE, the first recorded SBP was ≥ 140 mmHg in 52% of pts, and only 2% had a SBP < 90 mmHg. In contrast, baseline SBP in ADHF trials ranges from 106-121 mmHg. Pathophysiology and drug response in ADHF pts with elevated SBP may differ from pts with normal/low SBP. Nesiritide (NES) is a novel vasodilator that increases lusitropy and reduces filling pressure, peripheral arteriolar resistance, and systemic pressure. This profile may be associated with symptomatic or clinical benefit in hypertensive ADHF pts. This study will test the hypothesis that NES, initiated early, in ADHF pts presenting with SBP ≥ 140 mmHg safely lowers SBP, reduces symptoms, and improves biomarkers. Methods: UNDU ADHF-HTN is a prospective, multicenter, randomized, double-blind, placebo-controlled study. Pts with dyspnea at rest/minimal exertion within 3 hours (hrs) of ADHF presentation, pulmonary/systemic congestion, and SBP ≥ 140 mmHg at presentation (≥ 120 mmHg at randomization) will be enrolled. Major exclusions are STEMI, dialysis, NES contraindication, or non-cardiac pulmonary edema. Pts (n = 200) will be randomized 1:1 to NES or matching placebo (2 mg/kg IV bolus, then 0.01 mg/kg/min infusion for 48 hrs), on top of diuretics. IV furosemide ≤ 40 mg may be given before study drug. Subsequent diuretics will be given based on physician assessment. Pts given IV vasoactives after randomization will be considered treatment failures. Follow-up will be 180 days (d). The primary endpoint is change in SBP from baseline to 3 hrs. Secondary endpoints are change in SBP (24 hrs), change in NT-pro BNP (24 hrs), adverse outcome (worsening HF within 7 d or death at 30 d or HF rehospitalization at 30 d), symptomatic improvement (24 hrs), and total diuretic dose (48 hrs). Safety endpoints include change in estimated GFR, adverse events, and 180 d mortality. Mechanistic substudies will assess vascular compliance and neurohormones. Results: Enrollment start is planned for 08/07. Results are expected 1st quarter 2010. Conclusions: ADHF pts with HTN comprise half of the ADHF population, yet their pathophysiology is incompletely defined and no evidenced-based treatments specific to these pts are established. This study will evaluate the safety and efficacy of NES and will explore unique mechanisms that may precipitate ADHF or HF progression in hypertensive ADHF pts.

Intrathoracic impedance monitoring to detect chronic heart failure deterioration: Relationship to changes in NT‐proBNP

An alert algorithm, based on intrathoracic impedance monitoring, has been incorporated into a cardiac resynchronisation device (CRT) to detect pulmonary fluid accumulation, and to audibly alert patients to decompensating chronic heart failure (CHF). To evaluate this algorithm, alert events were correlated with changes in NT-proBNP concentration and CHF status. In a prospective observational study of 62 patients (89% male, aged 67+/-1 year), NT-proBNP plasma concentrations, clinical CHF status, and device data were collected at enrolment, during regular follow-up and at device alerts. Over a mean follow-up of 27+/-2 weeks, pooled data indicated a weak, but significant inverse relationship between relative changes in intrathoracic impedance and NT-proBNP (r=-0.3; p<0.001). In 52 device alerts from 35 patients, NT-proBNP increased by 66+/-19% from 2039+/-331 pg/ml (p<0.001). The increase in NT-proBNP was higher in alerts with clinical signs of CHF deterioration (n=30, 89+/-25%; p<0.001) than in alert events without clinical signs (n=22, 25+/-15%; p=n.s.). Intrathoracic impedance based alert events are associated with a significant increase in NT-proBNP concentration. These data indicate that intrathoracic impedance monitoring might facilitate the outpatient management of CHF patients with implanted CRT devices.

Perinatal Changes of Circulating N-Terminal Pro B-Type Natriuretic Peptide (NT-proBNP) in Normal and Intrauterine-Growth-Restricted Pregnancies

Objective: To investigate changes in NT-proBNP in intrauterine-growth-restricted (IUGR) and appropriate-for-gestational-age (AGA) pregnancies. Methods: NT-proBNP levels were measured in 40 mothers (MS), umbilical cords (UC), and their 20 IUGR/ 20 AGA neonates on day 1 (N1) and day 4 (N4). Results: UC, N1, and N4 NT-proBNP was lower in IUGR pregnancies (p ≤ 0.049). In both groups, NT-proBNP levels were similar in MS and higher in N1 (p ≤ 0.001). In AGA, MS NT-proBNP correlated positively with UC. Conclusions: Fetal and neonatal NT-proBNP levels are lower in IUGR compared with AGA, probably due to blood flow redistribution in IUGR and NT-proBNP placental transport in AGA. NT-proBNP levels peak on N1.

Changes in Plasma N-Terminal proBNP Levels and Ventricular Filling Pressures During Intensive Unloading Therapy in Elderly With Decompensated Congestive Heart Failure and Preserved Left Ventricular Systolic Function

Background Plasma B-type natriuretic peptide (BNP) levels depend on left ventricular (LV) filling pressures and correlate with the state of neurohormonal modulation in patients with congestive heart failure (CHF). In these subjects, therapy of decompensated CHF can determine acute changes in BNP levels. Methods and Results We defined the sequential pattern of N-terminal (T) proBNP in elderly with decompensated CHF and preserved LV systolic function undergoing intensive unloading therapy, assessed the prevalence of patients who significantly reduced NTproBNP at the end of treatment, and verified the relations between changes in NTproBNP and ventricular filling pressures. NTproBNP was measured in 30 patients hospitalized for worsening CHF with LV ejection fraction >50% at admission and after 2 to 4 and 6 to 8 days from the start of treatment. Patients who exhibited a reduction in NTproBNP >35% from baseline to 8-day evaluation were defined as “responders.” Twelve healthy subjects matched for age and sex were used as controls. NTproBNP was significantly higher in CHF patients than controls in all time points, to a greater extent in baseline evaluation (2982 [lower/upper quartile 1273/8146] versus 235 [150/280] pg/mL). A progressive, linear reduction of NTproBNP was detected in CHF patients during unloading. At Day 8, 18 patients (60%) resulted in “responders,” whereas 12 (40%) were “nonresponders.” The former could be predicted through higher pulmonary artery wedge pressure at baseline. Surprisingly, ventricular filling pressures similarly declined in responders and non responders. At Day 8, NTproBNP was yet 7-fold higher in CHF patients than controls. Conclusion Intensive unloading therapy is associated with a significant short-term reduction in NTproBNP in elderly with CHF and preserved LV systolic function. This behavior is progressive and linear during the first week and parallels a reduction in ventricular filling pressures which, however, does not differ between patients who significantly reduce NTproBNP and those who do not. Thus the short-term changes in NTproBNP during intensive unloading therapy in our patients do not depend only on the acute improvement in hemodynamic conditions.

B-type natriuretic peptides as powerful markers in cardiac diseases – analytical and clinical aspects / B-Typ natriuretische Peptide als aussagekräftige Marker bei kardialen Erkrankungen – analytische und klinische Aspekte

Abstract Among all natriuretic peptides and neurohormones, B-type natriuretic peptide (BNP) and its N-terminal prohormone fragment (NT-proBNP) have been shown to be the best and most powerful markers to identify patients with acute and chronic heart failure (HF). The fully automated BNP and NT-proBNP assays require only 15–20 min to achieve a test result so that a turn-around time of less than 60 min is possible, as requested by the guidelines of the cardiological societies. The in-vitro stabilities of BNP and NT-proBNP are sufficient for routine use. Most of the commercially available assays, except if they are sublicensed, use different antibodies. This may explain that in general, BNP and NT-proBNP assays show close correlations, but do not agree in absolute values. The assays have not been standardized so far and the application of various calibration materials may contribute to different results. Thus, reference ranges are dependent on the assay used, and reference ranges have to be determined for each assay separately. The increasing values with age may be related to the increasing frequency of subclinical renal or cardiac dysfunction in the elderly. Estrogens stimulate the natriuretic peptide production in females, and reference ranges depend on sex from adolescence to menopause. Immediately after birth, BNP and NT-proBNP levels are substantially higher in neonates than in their mothers. The high biological variation of natriuretic peptides must be considered when interpreting serial BNP and NT-proBNP results. Therefore, only marked BNP or NT-proBNP changes during follow-up are related to changes in the clinical HF status. A conclusion of all major studies is that in patients with chronic HF BNP and NT-proBNP are rather rule-out than rule-in markers because of limited cardiac specificities. Patients with acute HF usually show higher BNP and NT-proBNP levels than patients with chronic HF. The greatest efficiency of BNP and NT-proBNP testing was demonstrated in patients presenting to the emergency department with acute dyspnoea or in outpatients with symptoms suggesting chronic HF. Many studies indicate that short- and long-term prognosis in HF can be assessed by BNP or NT-proBNP determination. These hormones are independent predictors of death or HF hospitalizations. Natriuretic peptides are increased in all diseases affecting the cardiac or renal function and fluid balance. BNP and NT-proBNP are markers of cardiac dysfunction in patients with renal failure as well, but higher decision limits have to be used. Decreased BNP and NT-proBNP concentrations in obesity are not fully understood and controversial reports are found in the literature. In summary, BNP or NT-proBNP determination is a powerful test for ruling out HF. Furthermore, these markers are a useful addition to the standard clinical investigations of patients with suspected ventricular dysfunction.

P6-48: Cardiac resynchronization therapy induces simultaneous and identical (increase or decrease) changes of HS-CRP and NT-proBNP

P6-48: Cardiac resynchronization therapy induces simultaneous and identical (increase or decrease) changes of HS-CRP and NT-proBNP

B-type natriuretic peptides as powerful markers in cardiac diseases: Analytical and clinical aspects

Among all natriuretic peptides and neurohormones, B-type natriuretic peptide (BNP) and its Nterminal prohormone fragment (NT-proBNP) have been shown to be the best and most powerful markers to identify patients with acute and chronic heart failure (HF). The fully automated BNP and NT-proBNP assays require only 15-20 min to achieve a test result so that a turn-around time of less than 60 min is possible, as requested by the guidelines of the cardiological societies. The in-vitro stabilities of BNP and NT-proBNP are sufficient for routine use. Most of the commercially available assays, except if they are sublicensed, use different antibodies. This may explain that in general, BNP and NT-proBNP assays show close correlations, but do not agree in absolute values. The assays have not been standardized so far and the application of various calibration materials may contribute to different results. Thus, reference ranges are dependent on the assay used, and reference ranges have to be determined for each assay separately. The increasing values with age may be related to the increasing frequency of subclinical renal or cardiac dysfunction in the elderly. Estrogens stimulate the natriuretic peptide production in females, and reference ranges depend on sex from adolescence to menopause. Immediately after birth, BNP and NTproBNP levels are substantially higher in neonates than in their mothers. The high biological variation of natriuretic peptides must be considered when interpreting serial BNP and NT-proBNP results. Therefore, only marked BNP or NT-proBNP changes during follow-up are related to changes in the clinical HF status. A conclusion of all major studies is that in patients with chronic HF BNP and NT-proBNP are rather rule-out than rule-in markers because of limited cardiac specificities. Patients with acute HF usually show higher BNP and NT-proBNP levels than patients with chronic HF. The greatest efficiency of BNP and NT-proBNP testing was demonstrated in patients presenting to the emergency department with acute dyspnoea or in outpatients with symptoms suggesting chronic HF. Many studies indicate that short- and long-term prognosis in HF can be assessed by BNP or NT-proBNP determination. These hormones are independent predictors of death or HF hospitalizations. Natriuretic peptides are increased in all diseases affecting the cardiac or renal function and fluid balance. BNP and NT-proBNP are markers of cardiac dysfunction in patients with renal failure as well, but higher decision limits have to be used. Decreased BNP and NT-proBNP concentrations in obesity are not fully understood and controversial reports are found in the literature. In summary, BNP or NT-proBNP determination is a powerful test for ruling out HF. Furthermore, these markers are a useful addition to the standard clinical investigations of patients with suspected ventricular dysfunction.

NT-ProBNP in Acute Heart Failure: Correlation With Invasively Measured Hemodynamic Parameters During Recompensation

Background N-terminal brain natriuretic peptide (NT-proBNP) level is elevated in patients with acute and chronic heart failure. This study addresses whether NT-proBNP correlates with invasively measured hemodynamic parameters and whether a decrease of NT-proBNP over time correlates with invasively monitored hemodynamic improvement. Methods and Results Twenty consecutive patients with acute exacerbation of chronic heart failure (New York Heart Association class III-IV) were included in this prospective study. NT-proBNP and hemodynamic measurements by balloon-tipped pulmonary artery catheter were performed simultaneously. Recompensation strategies included vasodilators, diuretics, and inotropes. The patients were divided in 2 subgroups. Group A, by definition, had a hemodynamic improvement over 24 hours with an increase of cardiac index of >30% and a decrease of pulmonary capillary wedge pressure of >30%. Group B did not show a hemodynamic improvement. Group A had a decline of NT-proBNP levels to 42% of the baseline value over 32 hours. In group B, the NT-pro BNP levels did not change significantly over 32 hours. Conclusion The decrease of NT-proBNP correlates with hemodynamic improvement in patients with decompensated heart failure. The relative changes of NT-proBNP seem to be a reliable diagnostic tool in monitoring these patients. There results have been confirmed in a larger patient group.

Opposite effects of losartan and atenolol on natriuretic peptides in patients with hypertension and left ventricular hypertrophy: a LIFE substudy

Secretion of natriuretic peptides is related to cardiac wall stress and influenced by the renin-angiotensin system. Therefore, we investigated the influence of blood pressure (BP) reduction with losartan versus atenolol on N-terminal pro-atrial natriuretic peptide (Nt-proANP) and N-terminal pro-brain natriuretic peptide (Nt-proBNP). In 183 patients with hypertension and electrocardiographic left ventricular (LV) hypertrophy, enrolled in the LIFE Study, we measured BP and serum Nt-proANP and Nt-proBNP by immunoassay after 2 weeks of placebo treatment and after 1, 2, 4, 6, 12, 24, 36 and 48 months of randomized treatment with losartan- or atenolol-based antihypertensive regimens. There was no significant difference in BP at any time point between the two treatment groups. In patients treated with losartan, median Nt-proANP decreased gradually throughout the study, reaching significance after 6 months of treatment (1125-1060 pmol/l, P < 0.001), and Nt-proBNP decreased within the first month (24.7-18.7 pmol/l, P < 0.01) and stayed reduced throughout the study. During losartan-based antihypertensive treatment, Nt-proANP and Nt-proBNP as a percentage of baseline values were correlated to reductions in systolic BP (r = 0.11, P < 0.01 and r = 0.10, P = 0.01) and diastolic BP (r = 0.17, P < 0.001 and r = 0.07, P = 0.09). In atenolol-treated patients, Nt-proANP (1100-1640 pmol/l, P < 0.001) and Nt-proBNP (20.0-37.7 pmol/l, P < 0.001) increased during the first month, and remained elevated throughout the study. During atenolol-based antihypertensive treatment, changes in Nt-proANP (r = -0.16, P < 0.001) and Nt-proBNP (r = -0.07, P = 0.08) were negatively related to change in heart rate. Nt-proANP and Nt-proBNP were reduced in parallel with BP in losartan-treated patients whereas they increased in parallel with decreased heart rate in atenolol-treated patients.

Levosimendan reduces plasma B-type natriuretic peptide and interleukin 6, and improves central hemodynamics in severe heart failure patients

Background: Plasma B-type natriuretic peptide (BNP) and interleukin 6 (IL-6) levels have recently been demonstrated as significant neurohormonal markers associated with the progression of chronic heart failure (CHF). Additionally, clinical studies have shown that the calcium sensitizer, levosimendan, beneficially affects the central hemodynamics of CHF patients and improves their long-term prognosis. This study investigates whether levosimendan-induced hemodynamic improvement of CHF patients is related to the respective changes of NT-proBNP and IL-6 levels. Methods: Circulating levels of NT-pro BNP and IL-6 were measured by enzyme-linked immunosorbent assay (ELISA) in 12 patients with decompensated advanced CHF at baseline, immediately after the end of a 24-h levosimendan infusion and 72 h after the initiation of treatment. Hemodynamic parameters of patients (pulmonary wedge and pulmonary artery pressure (PAP), systemic and pulmonary vascular resistance (PVR), stroke volume, and cardiac output and index) were also monitored during the same period. Results: NT-proBNP and IL-6 levels were significantly reduced in severe CHF patients within 72 h after the initiation of levosimendan treatment ( p<0.01 and p<0.05, respectively). A significant reduction of pulmonary wedge ( p<0.01) and artery pressure values ( p<0.05) was also found during the same period. A good correlation between the levosimendan-induced changes in NT-proBNP levels and the respective reduction of pulmonary wedge pressure ( r s=0.65, p<0.05) was observed. Conclusions: Our results indicate that changes of NT-pro BNP and IL-6 levels may be useful biochemical markers related with the levosimendan-induced improvement in central hemodynamics and the clinical status of decompensated advanced CHF patients.

Application of determined NT-proBNP in physical standardized exercise.

Natriuretic peptides can be used as markers of heart failure, its severity and also in the differential diagnosis of dyspnea. Moreover, the dynamics of natriuretic peptides in physical standardized exercise may be used in the assessment of latent heart failure. Can determination of NT-proBNP be used in the diagnosis of exercise-induced ischemia or latent heart failure? 18 probands (10 men, 8 women) under study were risk persons with unspecified ECG, without signs of manifest heart failure. They were subjected to ergometric bike exercises up to the subjective maximum, SPECT myocardium with estimated ejection fraction of the left ventricle at peak ergometric exercise. The following parameters were followed-up: a) before ergometric exercise: NT-proBNP, CRP, TNF-alpha, Hb, Htc, lactate b) at subjective maximum: NT-proBNP, Hb, Htc, lactate c) 30 min after stopping the exercise: NT-proBNP d) 60 min after stopping the exercise: NT-proBNP. The volume blood changes were taken into account (estimation from the dynamics of Htc, Hb with calculation of metabolic changes of NT-proBNP). To evaluate the dynamics of NT-proBNP, the group was divided into subgroups according to the results obtained in ergometric exercises. initial values of NT-proBNP within normal limits (< 59 pmol/l, 500 ng/l) in 94%, the submaximal pulse rate was reached in 94%, ischemic changes in ECG were observed in 59%, typical clinical signs of heart ischemia were recorded in 35%. Signs of heart dysfunction according to SPECT were found in 47% and ischemic symptoms were observed in 43%. In general, the plasmatic volume decreased by 24% at maximal exercise. Lactate concentration in the plasma increased in all cases. Conversion of NT-proBNP into volume blood changes revealed that increased NT-proBNP occurred only in 22%. Differences between NT-proBNP before exercises and at maximal exercise prior and after correction into volume blood changes were statistically insignificant. 30 and 60 min after the exercise, no significant differences were found in NT-proBNP concentrations. Dividing into subgroups according to the results of ergometric exercises, showed no significant differences in NT-proBNP concentrations. Dynamics of NT-proBNP changes during and after ergometric exercises cannot be used for the diagnosis of exercise-induced heart failure. The high stability of NT-proBNP related to physical activity was confirmed.